Linoleoyl ethanolamide reduces lipopolysaccharide-induced inflammation in macrophages and ameliorates 2,4-dinitrofluorobenzene-induced contact dermatitis in mice

Ishida, Tatsuro; Nishiumi, Shin; Tanahashi, Takao; Yamasaki, Akifumi; Yamazaki, Asahi; Akashi, Takahiro; Miki, Ikuya; Kondo, Yasuyuki; Inoue, Jun; Kawauchi, Shoji; Azuma, Takeshi; Yoshida, Masaru; Mizuno, Shigeto

doi:10.1016/j.ejphar.2012.11.030

Cited by 43 publications

(30 citation statements)

References 41 publications

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“…Likewise, linoleoyl ethanolamide, palmitoleoyl ethanolamide, N,N-Dimethylsphingosine and quinolinic acid (Figure 5B), were significantly changed in saccharin-treated mice. The effects of these compounds in mediating inflammation have been demonstrated in previous studies (Ishida et al, 2013; Nishiuma et al, 2008). …”

Section: Resultssupporting

confidence: 56%

“…As a fatty acid ethanolamide, PEA was found to inhibit inflammation in human adipocytes and peripheral tissues through the regulation of pro-inflammatory proteins, nitric oxide, and neutrophils (Ezzili, Otrubova, & Boger, 2010). Likewise, LEA was reported to reduce LPS-induced inflammation in macrophages (Ishida et al, 2013). N,N-Dimethylsphingosine was shown to attenuate airway inflammation in a mouse model (Nishiuma et al, 2008).…”

Section: Discussionmentioning

confidence: 99%

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Saccharin induced liver inflammation in mice by altering the gut microbiota and its metabolic functions

Bian

Chi

et al. 2017

Food and Chemical Toxicology

156

123

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Maintaining the balance of the gut microbiota and its metabolic functions is vital for human health, however, this balance can be disrupted by various external factors including food additives. A range of food and beverages are sweetened by saccharin, which is generally considered to be safe despite controversial debates. However, recent studies indicated that saccharin perturbed the gut microbiota. Inflammation is frequently associated with disruptions of the gut microbiota. The aim of this study is to investigate the relationship between host inflammation and perturbed gut microbiome by saccharin. C57BL/6J male mice were treated with saccharin in drinking water for six months. Q-PCR was used to detect inflammatory markers in mouse liver, while 16S rRNA gene sequencing and metabolomics were used to reveal changes of the gut microbiota and its metabolomic profiles. Elevated expression of pro-inflammatory iNOS and TNF-α in liver indicated that saccharin induced inflammation in mice. The altered gut bacterial genera, enriched orthologs of pathogen-associated molecular patterns, such as LPS and bacterial toxins, in concert with increased pro-inflammatory metabolites suggested that the saccharin-induced liver inflammation could be associated with the perturbation of the gut microbiota and its metabolic functions.

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Section: Resultssupporting

confidence: 56%

Section: Discussionmentioning

confidence: 99%

Saccharin induced liver inflammation in mice by altering the gut microbiota and its metabolic functions

Bian

Chi

et al. 2017

Food and Chemical Toxicology

156

123

View full text Add to dashboard Cite

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“…Although these EC-like ligands cannot bind to cannabinoid receptors with high affinity, they may influence endocannabinoid function via competition for catabolic enzymes 42 . It has been reported that EC-like ligands show anti-inflammatory, analgesic, anticonvulsant and neuroprotective properties 43–46 . Moreover, OEA can regulate feeding and body weight 47 .…”

Section: Disscussionmentioning

confidence: 99%

Simvastatin and Bezafibrate ameliorate Emotional disorder Induced by High fat diet in C57BL/6 mice

Wang

Zhou

Liu

et al. 2017

Sci Rep

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High fat diet (HFD)-induced metabolic disorders may lead to emotional disorders. This study aimed to explore the effect of simvastatin (SMV) and bezafibrate (BZ) on improving HFD-induced emotional changes, and tried to identify their different mechanisms. The intraperitoneal glucose tolerance test (IPGTT) was used to evaluate glucose control ability; and behavior tests including open field tests (OFT), forced swimming tests (FST), tail suspension tests (TST) and sucrose preference (SPT), were then performed to evaluate emotional changes. Serum samples were collected for the LC-MS based metabolomics analysis to explore the emotional-related differential compounds; we then evaluated the effect of the drugs. The abnormal serum metabolic profiling and emotional changes caused by HFD in mice was alleviated by SMV treatment, whereas BZ only affected the emotional disorder. The improvement of cannabinoid analogues and then produced influences on the endocannabinoid system, which may be a potential mechanism SMV action. BZ promoted tryptophan-serotonin pathway and inhibited tryptophan-kynurenine pathway, which may be its mechanism of action. Here, we proposed a shed light on the biological mechanisms underlying the observed effects, and identified an important drug candidate for the treatment of emotional disorders induced by HFD.

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“…However, it is not known whether PEA affects COX‐2 expression or PG production in LPS‐stimulated macrophages, akin to that seen for the PEA homologues docosahexaenoylethanolamide (DHEA) and linoleoylethanolamide (LEA) (Ishida et al. ; Meijerink et al. ).…”

Section: Introductionmentioning

confidence: 99%

“…Thus, PEA can affect the function of macrophages and can reduce in vivo the COX-2 induction following inflammation produced by LPS. However, it is not known whether PEA affects COX-2 expression or PG production in LPS-stimulated macrophages, akin to that seen for the PEA homologues docosahexaenoylethanolamide (DHEA) and linoleoylethanolamide (LEA) (Ishida et al 2013;Meijerink et al 2015). In consequence, we have investigated the effects of PEA upon COX expression and PG production in LPS + interferon-c (IFNc)-treated RAW264.7 macrophages.…”

Section: Introductionmentioning

confidence: 99%

The anti-inflammatory compound palmitoylethanolamide inhibits prostaglandin and hydroxyeicosatetraenoic acid production by a macrophage cell line

Gabrielsson

Gouveia-Figueira

Häggström

et al. 2017

Pharmacol Res Perspect

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The anti‐inflammatory agent palmitoylethanolamide (PEA) reduces cyclooxygenase (COX) activity in vivo in a model of inflammatory pain. It is not known whether the compound reduces prostaglandin production in RAW264.7 cells, whether such an action is affected by compounds preventing the breakdown of endogenous PEA, whether other oxylipins are affected, or whether PEA produces direct effects upon the COX‐2 enzyme. RAW264.7 cells were treated with lipopolysaccharide and interferon‐γ to induce COX‐2. At the level of mRNA, COX‐2 was induced >1000‐fold following 24 h of the treatment. Coincubation with PEA (10 μmol/L) did not affect the levels of COX‐2, but reduced the levels of prostaglandins D2 and E2 as well as 11‐ and 15‐hydroxyeicosatetraenoic acid, which can also be synthesised by a COX‐2 pathway in macrophages. These effects were retained when hydrolysis of PEA to palmitic acid was blocked. Linoleic acid‐derived oxylipin levels were not affected by PEA. No direct effects of PEA upon the oxygenation of either arachidonic acid or 2‐arachidonoylglycerol by COX‐2 were found. It is concluded that in lipopolysaccharide and interferon‐γ‐stimulated RAW264.7 cells, PEA reduces the production of COX‐2‐derived oxylipins in a manner that is retained when its metabolism to palmitic acid is inhibited.

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Linoleoyl ethanolamide reduces lipopolysaccharide-induced inflammation in macrophages and ameliorates 2,4-dinitrofluorobenzene-induced contact dermatitis in mice

Cited by 43 publications

References 41 publications

Saccharin induced liver inflammation in mice by altering the gut microbiota and its metabolic functions

Saccharin induced liver inflammation in mice by altering the gut microbiota and its metabolic functions

Simvastatin and Bezafibrate ameliorate Emotional disorder Induced by High fat diet in C57BL/6 mice

The anti-inflammatory compound palmitoylethanolamide inhibits prostaglandin and hydroxyeicosatetraenoic acid production by a macrophage cell line

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